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Mitochondria Theory, Part Two [Logged in view]
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2005-02-07 19:19:57
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The Mitochondria Theory; Part Two
In order for the mitochondria to survive, it requires oxygen, supplied by the nucleus, thus forming a symbiotic relationship. The way our cells are set up, if the amount energy processed in the cells remained abundant, we would not age much past our prime due to the constant regeneration of live cells. It is actually the inefficiency of mitochondra, called Mitochondrian Aging that causes aging and eventual death.
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"Mitochondrial electron transport is not perfect. Even under ideal conditions, some electrons “leak” from the electron transport chain. These leaking electrons interact with oxygen to produce superoxide radicals. With mitochondrial dysfunction, leakage of electrons can increase significantly. The close proximity of mtDNA to the flux of superoxide radicals (or hydroxyl radicals), and it’s lack of protection and repair mechanisms, leads to free radical-mediated mutations and deletions. Mitochondrial aging has been proposed as an underlying cause of 1) free-radical stress, 2) degenerative disease and 3) aging (Miguel, 1980, 1991, 1992, Shigenaga et al., 1994).
Evidence is accumulating that mitochondrial dysfunction underlies many common pathologies. Mitochondrial defects have been identified in Parkinson’s disease, Alzheimer’s disease (Hutchin and Cortopassi, 1995), heart disease, fatigue syndromes, numerous genetic conditions, and nucleoside therapy for AIDS. Also, many common nutritional deficiencies can impair mitochondrial efficiency.
At this time, the degree of mitochondrial involvement in age-related mental decline (ARMD) and age-associated memory impairment (AAMI) is not known. A significant amount of the mitochondrial DNA (mtDNA) damage seen in Parkinson’s disease is also observed in age-matched controls. Such observations suggest that reductions in mitochondrial efficiency and ATP output may underlie many age-associated phenomena. The successful use of mitochondrial support nutrients to ameliorate serious mitochondrial diseases may prove to be generalizable to the subclinical complaints of normal, healthy, aging humans."]
For scientists of microbiology and genetics, there is a commonly believed theory which states that the fundamental genetic instinct is suvival of the species. According to microbiology, the nucleus and the mitochondria of the cell are dependant upon one another for survival. But this wasn't always so.
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"One interesting property of mitochondria is that they have their own DNA (deoxyribonucleic acid), the stuff of which genes and chromosomes are made. Mitochondrial DNA (mtDNA) is quite different from nuclear DNA in several respects. First, it exists as a simple plasmid (a DNA loop), and in this respect, it is more akin to bacterial DNA than the chromosomal DNA of higher organisms. Second, mtDNA is not associated with histones. Histones are positively charged “storage” proteins around which nuclear DNA is wound for safekeeping (like thread on a spool). Third, most of the complex DNA repair mechanisms that correct damage to nuclear DNA are missing from mitochondria. All of these features have prompted some scientists to speculate that mitochondria are ancient remnants of primitive symbiotic bacteria. Whether this view is correct or not, the relatively unprotected and unrepaired mtDNA suffers more than ten times the damage that nuclear DNA does (Miguel, 1991, 1992; Shigenaga et al., 1994). This leads to mitochondrial dysfunction, disruption of cellular energy production, and accelerated cellular aging (Miguel, 1980)."]
By this statement we can assume that at some point mitochondria evolved into their current productive state. Also we know that the mitochondria carry their own DNA, thus making genetic evolution possible still.
By these facts and the genetic law stated above, one could hypothesize that the mitochondria might evolve in for the sake of survival.
Perhaps a person is born with a biological malfunction. Examples: There cells did not contain enough mitochondria, or perhaps the nuclei of their cells were not supplying enough oxygen to the mitochondria. It would be assumed that any being under these circumstances would die...perhaps never even be born. But what if, as happened in the past, the mitochondria began to evolve to ensure survival? What if the cells themselves began to seek other ways to absorb the energy that means continuance?
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